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A truncated NLR protein, TIR-NBS2, is required for activated defense responses in the exo70B1 mutant.

Zhao T, Rui L, Li J, Nishimura MT, Vogel JP, Liu N, Liu S, Zhao Y, Dangl JL, Tang D - PLoS Genet. (2015)

Bottom Line: Our study thus provides a link between the exocyst complex and the function of a 'TIR-NBS only' immune receptor like protein.Our data are consistent with a speculative model wherein pathogen effectors could evolve to target EXO70B1 to manipulate plant secretion machinery.TN2 could monitor EXO70B1 integrity as part of an immune receptor complex.

View Article: PubMed Central - PubMed

Affiliation: The State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.

ABSTRACT
During exocytosis, the evolutionarily conserved exocyst complex tethers Golgi-derived vesicles to the target plasma membrane, a critical function for secretory pathways. Here we show that exo70B1 loss-of-function mutants express activated defense responses upon infection and express enhanced resistance to fungal, oomycete and bacterial pathogens. In a screen for mutants that suppress exo70B1 resistance, we identified nine alleles of TIR-NBS2 (TN2), suggesting that loss-of-function of EXO70B1 leads to activation of this nucleotide binding domain and leucine-rich repeat-containing (NLR)-like disease resistance protein. This NLR-like protein is atypical because it lacks the LRR domain common in typical NLR receptors. In addition, we show that TN2 interacts with EXO70B1 in yeast and in planta. Our study thus provides a link between the exocyst complex and the function of a 'TIR-NBS only' immune receptor like protein. Our data are consistent with a speculative model wherein pathogen effectors could evolve to target EXO70B1 to manipulate plant secretion machinery. TN2 could monitor EXO70B1 integrity as part of an immune receptor complex.

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exo70B1-3 mutants display enhanced resistance to H.a. Noco2, Pto DC3000 and Pto DC3000 avrRpt2.(A) Two-week-old seedlings were inoculated with H.a. Noco2. The number of spores was counted at 7 dpi. The asterisk indicates a significant difference from WT (p < 0.01; Student’s t-test). (B)-(C) Four-week-old plants were infiltrated with Pto DC3000 (B) and Pto DC3000 avrRpt2(C). Bacterial growth was monitored at 0 and 3 dpi. cfu: colony-forming units. The asterisk indicates a significant difference from wild type (p < 0.01; Student’s t-test). Bars represent mean and standard deviation of values from three biological samples. The experiments were repeated three times with similar results.
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pgen.1004945.g004: exo70B1-3 mutants display enhanced resistance to H.a. Noco2, Pto DC3000 and Pto DC3000 avrRpt2.(A) Two-week-old seedlings were inoculated with H.a. Noco2. The number of spores was counted at 7 dpi. The asterisk indicates a significant difference from WT (p < 0.01; Student’s t-test). (B)-(C) Four-week-old plants were infiltrated with Pto DC3000 (B) and Pto DC3000 avrRpt2(C). Bacterial growth was monitored at 0 and 3 dpi. cfu: colony-forming units. The asterisk indicates a significant difference from wild type (p < 0.01; Student’s t-test). Bars represent mean and standard deviation of values from three biological samples. The experiments were repeated three times with similar results.

Mentions: To examine whether exo70B1-3 causes resistance to other pathogens, we challenged exo70B1-3 with the virulent oomycete pathogen Hyaloperonospora arabidopsidis (H. a.) Noco2 and the bacterial pathogen Pseudomonas syringae pv. tomato (Pto) DC3000. Two-week old seedlings were infected with H.a. Noco2, and we found that exo70B1-3 supported significantly fewer spores than the wild type at 7 dpi (Fig. 4A). Similarly, exo70B1-3 were more resistant to the virulent strain Pto DC3000 and the avirulent bacterial strain Pto DC3000 avrRpt2 (Fig. 4B, 4C).


A truncated NLR protein, TIR-NBS2, is required for activated defense responses in the exo70B1 mutant.

Zhao T, Rui L, Li J, Nishimura MT, Vogel JP, Liu N, Liu S, Zhao Y, Dangl JL, Tang D - PLoS Genet. (2015)

exo70B1-3 mutants display enhanced resistance to H.a. Noco2, Pto DC3000 and Pto DC3000 avrRpt2.(A) Two-week-old seedlings were inoculated with H.a. Noco2. The number of spores was counted at 7 dpi. The asterisk indicates a significant difference from WT (p < 0.01; Student’s t-test). (B)-(C) Four-week-old plants were infiltrated with Pto DC3000 (B) and Pto DC3000 avrRpt2(C). Bacterial growth was monitored at 0 and 3 dpi. cfu: colony-forming units. The asterisk indicates a significant difference from wild type (p < 0.01; Student’s t-test). Bars represent mean and standard deviation of values from three biological samples. The experiments were repeated three times with similar results.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4305288&req=5

pgen.1004945.g004: exo70B1-3 mutants display enhanced resistance to H.a. Noco2, Pto DC3000 and Pto DC3000 avrRpt2.(A) Two-week-old seedlings were inoculated with H.a. Noco2. The number of spores was counted at 7 dpi. The asterisk indicates a significant difference from WT (p < 0.01; Student’s t-test). (B)-(C) Four-week-old plants were infiltrated with Pto DC3000 (B) and Pto DC3000 avrRpt2(C). Bacterial growth was monitored at 0 and 3 dpi. cfu: colony-forming units. The asterisk indicates a significant difference from wild type (p < 0.01; Student’s t-test). Bars represent mean and standard deviation of values from three biological samples. The experiments were repeated three times with similar results.
Mentions: To examine whether exo70B1-3 causes resistance to other pathogens, we challenged exo70B1-3 with the virulent oomycete pathogen Hyaloperonospora arabidopsidis (H. a.) Noco2 and the bacterial pathogen Pseudomonas syringae pv. tomato (Pto) DC3000. Two-week old seedlings were infected with H.a. Noco2, and we found that exo70B1-3 supported significantly fewer spores than the wild type at 7 dpi (Fig. 4A). Similarly, exo70B1-3 were more resistant to the virulent strain Pto DC3000 and the avirulent bacterial strain Pto DC3000 avrRpt2 (Fig. 4B, 4C).

Bottom Line: Our study thus provides a link between the exocyst complex and the function of a 'TIR-NBS only' immune receptor like protein.Our data are consistent with a speculative model wherein pathogen effectors could evolve to target EXO70B1 to manipulate plant secretion machinery.TN2 could monitor EXO70B1 integrity as part of an immune receptor complex.

View Article: PubMed Central - PubMed

Affiliation: The State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.

ABSTRACT
During exocytosis, the evolutionarily conserved exocyst complex tethers Golgi-derived vesicles to the target plasma membrane, a critical function for secretory pathways. Here we show that exo70B1 loss-of-function mutants express activated defense responses upon infection and express enhanced resistance to fungal, oomycete and bacterial pathogens. In a screen for mutants that suppress exo70B1 resistance, we identified nine alleles of TIR-NBS2 (TN2), suggesting that loss-of-function of EXO70B1 leads to activation of this nucleotide binding domain and leucine-rich repeat-containing (NLR)-like disease resistance protein. This NLR-like protein is atypical because it lacks the LRR domain common in typical NLR receptors. In addition, we show that TN2 interacts with EXO70B1 in yeast and in planta. Our study thus provides a link between the exocyst complex and the function of a 'TIR-NBS only' immune receptor like protein. Our data are consistent with a speculative model wherein pathogen effectors could evolve to target EXO70B1 to manipulate plant secretion machinery. TN2 could monitor EXO70B1 integrity as part of an immune receptor complex.

Show MeSH
Related in: MedlinePlus